Direct bilirubin and the neutrophil-to-monocyte ratio timely predict intensive care unit admission in patients with severe acute respiratory syndrome coronavirus-2 infection (COVID-19)

Objective: Intensive care units (ICUs) collapsed under the global wave of coronavirus disease 2019 (COVID-19). Thus, we designed a clinical decision-making model that can help predict at hospital admission what patients with COVID-19 are at higher risk of requiring critical care. Method(s): This was a cross-sectional study in 119 patients that met hospitalization criteria for COVID-19 including less than 30 breaths per minute, peripheral oxygen saturation < 93%, and/or >= 50% lung involvement on imaging. Depending on the need for critical care, patients were retrospectively assigned to ICU and non-ICU groups. Demographic, clinical, and laboratory parameters were collected at admission and analyzed by classification and regression tree (CRT). Result(s): Forty-five patients were admitted to ICU and 80% of them were men older than 57.13 +/- 12.80 years on average. The leading comorbidity in ICU patients was hypertension. The CRT revealed that direct bilirubin (DB) > 0.315 mg/dl together with the neutrophil-to-monocyte ratio (NMR) > 15.90 predicted up to correctly in 92% of the patients the requirement of intensive care management, with sensitivity of 93.2%. Preexisting comorbidities did not influence on the tree growing. Conclusion(s): At hospital admission, DB and NMR can help identify nine in 10 patients with COVID-19 at higher risk of ICU admission.Copyright © 2022 Sociedad Medica del Hospital General de Mexico.

Cool Your Jets Bro

History: Twenty-two year old male basic trainee was brought to the ED after collapsing during a routine ruck march. At mile 8/12, soldier was noted to develop an unsteady gate and had witnessed loss of consciousness. A rectal core temperature was obtained and noted to be >107degreeF. Cooling initiated with ice sheets and EMS was activated. On arrival to the ED, patient demonstrated confusion and persistently elevated core temperatures despite ice sheeting, chilled saline and cold water bladder lavage. Cooling measures were discontinued after patient achieved euthermia in the ED;however, his temperatures subsequently spiked>103degreeF. Given rebound hyperthermia, an endovascular cooling (EVC) device was placed in the right femoral vein and patient was transferred to the ICU. Multiple attempts to place EVC device on standby were unsuccessful with subsequent rebound hyperthermia. Prolonged cooling was required. Physical Exam: VS: HR 121, BP 85/68, RR 22 SpO2 100% RA, Temp 102.4degreeF Gen: young adult male, NAD, shivering, A&Ox2 (person and place only) HEENT: Scleral anicteric, conjunctiva non-injected, moist mucus membranes Neck: Supple, no LAD Chest: CTAB, no wheezes/rales/rhonchi CV: tachycardia, regular rhythm, normal S1, S2 without murmurs, rubs, gallops ABD: NABS, soft/non-distended, no guarding or rebound EXT: No LE edema, tenderness SKIN: blisters with broad erythematous bases on bilateral heels Neuro: CN II-XII grossly intact, 5/5 strength in all extremities. Differential Diagnosis: 216. Septic Shock 217. Hypothalamic Stroke 218. Exertional Heat Stroke (EHS) 219. Neuroleptic Malignant Syndrome 220. Thyroid Storm Test Results: CBC: 18.2>14.5/40.6<167 CMP: 128/3.5 88/1831/2.7<104, AST 264, ALT 80, Ca 8.8 Lactate: 7.1 CK: 11 460 Myoglobin: 18 017 TSH: 3.16 CXR: No acute cardiopulmonary process Blood Cx: negative x2 CSF Cx: Negative COVID/Influenza/EBV: Negative Brain MRI: wnl. Final Diagnosis: Exertional Heat Stroke. Discussion(s): No EVC protocols exist for the management of EHS or rebound/refractory hyperthermia. As a result, the protocol used for this patient was adapted from post-cardiac arrest cooling protocols. It is unclear if this adapted protocol contributed to his delayed cooling and rebound hyperthermia as it was not intended for this patient demographic/ pathophysiology. Furthermore, despite initiating empiric antibiotics upon admission, delayed recognition and tailored therapy for his bilateral ankle cellulitis may have contributed to the difficulty in achieving euthermia. In summary, more research needs to be done to evaluate and develop an EVC protocol for EHS. Outcome(s): Euthermia was achieved and maintained after 36 hours of continuous EVC, at which point it was discontinued. His CK, AST/ALT, creatinine and sodium down-trended after discontinuation of EVC. Patient's antibiotics were transitioned to an oral formulation for treatment of ankle cellulitis and he was prepared for discharge. He was discharged with regular follow-up with the Fort Benning Heat Clinic. Follow-Up: After discharge, patient had regularly scheduled visits with the Fort Benning Heat Clinic. His typical lab markers for exertional heat stroke were regularly monitored. He had continued resolution of his Rhabdomyolysis, acute kidney injury and hyponatremia with typical treatment. Soldier returned to duty after 10 weeks of close monitoring and rehabilitation.

Clinical and laboratory characteristics of the COVID-19 disease in adult patients

BACKGROUND: In December 2019, a new coronavirus, SARS-CoV-2, appeared in Wuhan, China. This virus is the cause of the COVID-19 disease. This infection later spread to the whole world. The goal of this article is to present the clinical and laboratory characteristics of patients with COVID-19 treated in the Faculty Hospital Pilsen. METHOD(S): In this monocentric, retrospective study, clinical and biochemical data of 89 adult patients with COVID-19 was analyzed. These patients were in the care of the Faculty Hospital Pilsen between March 14 and April 7. RESULT(S): In this cohort, made up of 89 patients, 63 were treated as outpatients and 26 were hospitalized. 10 patients required intensive care. The most common symptoms among patients were cough and fever. Dyspnea was present in 29 patients. A CT scan showed bilateral pneumonia in 23 of the admitted patients. Fever and bilateral pneumonia were significantly more common in patients >= 60 years old (p=0.047, and p=0.001, respectively). Of lab results, the patients in intensive care had significantly higher values of C-reactive protein, procalcitonin, lactate dehydrogenase, interleukin 6, myoglobin and ferritin. CONCLUSION(S): The most common symptoms of COVID-19 are fever and cough. These two symptoms are simultaneously present in more than half the cases. Approximately 1/10th of patients requires intensive care. Higher values of lactate dehydrogenase, myoglobin and ferritin on patient admission appear to be a strong predictive factor of the patient's status progressing into requiring ICU attention.Copyright © 2020 Neuroendocrinology Letters

Myositis Associated with the Anti-COVID-19 Covishield Vaccine

Introduction: The SARS-CoV-2 made the world stop its activities, and the only chance of returning to normal life is the vaccine. But like any vaccination, some complications have been reported. We report the case of a patient who presented a myositis following the administration of the Covishield* (AZD1222, ChAdOx1 nCoV-19, AstraZeneca) COVID-19 vaccine. Case Report: 12 hours after his first dose, an 84-year-old patient presented to us reporting a decrea-sed muscle strength: the patient can move against gravity but not against resistance. The biological assessment showed that CK was at 4,250 IU/L, myoglobin was at 144 microgram/L and aldolases at 16.9 U/L. The patient received high doses of corticosteroids. Discussion(s): The development of vaccines and immunization programs reduced the morbidity and mortality of several diseases. Other case reports suggested the possible association between myopathies and the administration of the hepatitis B vaccine and H1N1 plus the seasonal trivalent influenza and other vaccines. The exact mechanism is still unknown, but a presumable autoimmune phe-nomenon is incriminated. Conclusion(s): The main purpose of this case report is to raise awareness about the possible link between the COVID-19 vaccination and polymyositis and the urge to take charge to avoid further complications.Copyright © 2023 Bentham Science Publishers.

Investigating Biomarkers for COVID-19 Morbidity and Mortality.

BACKGROUND AND OBJECTIVE: This retrospective study aims to disclose further early parameters of COVID-19 morbidity and mortality. METHODS: Three hundred and eighty-two COVID-19 patients, recruited between March and April 2020, were divided into three groups according to their outcome: (1) hospital ward group (patients who entered the hospital wards and survived); (2) intensive care unit (ICU) group (patients who attended the ICU and survived); (3) the deceased group (patients admitted to ICU with a fatal outcome). We investigated routine laboratory parameters such as albumin, glycemia, hemoglobin amylase, lipase, AST, ALT, GGT, LDH, CK, MGB, TnT-hs, IL-6, ferritin, CRP, PCT, WBC, RBC, PLT, PT, INR, APTT, FBG, and D-dimer. Blood withdrawal was carried out at the beginning of the hospitalization period. RESULTS: ANOVA and ROC data evidenced that the concomitant presence of alterations in albumin, lipase, AST, ALT, LDH, MGB, CK, IL-6, ferritin in women, CRP and D-dimer is an early sign of fatal outcomes. CONCLUSION: The present study confirms and extends the validity of routine laboratory biomarkers (i.e., lipase, AST, ALT, LDH, CK, IL-6, ferritin in women, CRP and D-dimer) as indicators of COVID-19 morbidity and mortality. Furthermore, the investigation suggests that both gross changes in albumin and MGB, markers of liver and heart damage, may early disclose COVID-19 fatal outcomes.

Myoglobin and troponin as prognostic factors in patients with COVID-19 pneumonia.

BACKGROUND: The outbreak of novel coronavirus pneumonia 2019 (COVID-19) has caused millions of deaths worldwide. It is well documented that troponin predicts the prognosis of patients. Myoglobin is not only an important marker of myocardial injury, but it indicates systemic muscle damage. However, its relationship with COVID-19 was rarely reported. The present study compared the predictive value of troponin and myoglobin on the final prognosis of COVID-19 patients by analyzing the clinical characteristics and serum levels of myoglobin and troponin in severe/critical COVID-19 patients. METHODS: We enrolled 499 consecutive eligible hospitalized patients with severe/critical COVID-19 from February 14 to March 24, 2020 at Leishenshan Hospital, Wuhan, China. Clinical characteristics and laboratory data were collected and compared between the patients who died and survived. We analyzed the receiver operating characteristic curves of myoglobin and troponin. Then, the patients were divided into myo+ group, myo- group, tro+ group, and tro- group, and survival curves were analyzed. The prognostic predictable values of myoglobin and troponin were further analyzed using Cox multifactorial analysis. RESULTS: Myoglobin and troponin were significantly elevated in the death group (134.4 [interquartile range (IQR) 24.80, 605] vs 38.02 [IQR 3.87, 11.73] ng/ml, p < 0.001), and troponin was also significantly elevated in the death group (0.01 [IQR 0.01, 0.01] vs 0.04 [IQR 0.02, 0.15] ng/ml, p < 0.001). The ROC curves demonstrated that the area under the curve when using myoglobin to predict patient death was 0.911, with a threshold of 1.17, which was equivalent to troponin. Kaplan-Meier survival analysis revealed a significantly lower survival curve in the myo+ group than the myo- group. Multifactor Cox survival analysis showed that troponin was no longer significant (HR = 0.98, 95% CI 0.92-1.03, p = 0.507), but elevated myoglobin was an independent predictor of death in COVID-19 patients (HR = 1.001, 95% CI 1.001-1.002, p < 0.001). The analysis of the Cox model for predicting patient death and plotting decision curves suggested that the single factor myoglobin model was superior to troponin, and the predictive value of the multifactor model was superior to the single-factor analyses. CONCLUSIONS: In severe/critical COVID-19 patients, myoglobin and troponin were predictors of mortality and the probability of conversion to critical illness, and myoglobin may be superior to troponin for predictive value.

ANTECEDENTES: El brote de la nueva neumonía por coronavirus 2019 (COVID-19) ha causado millones de muertes en todo el mundo. Está bien documentado que la troponina predice el pronóstico de los pacientes. La mioglobina no solo es un importante marcador de lesión miocárdica, sino que indica daño muscular sistémico. Sin embargo, su relación con la COVID-19 ha sido raramente comunicada. En el presente estudio se ha comparado el valor predictivo de la troponina y la mioglobina en el pronóstico final de los pacientes con COVID-19, analizando las características clínicas y los niveles séricos de mioglobina y troponina en pacientes con COVID-19 en estado grave o crítico. MÉTODOS: Se inscribió a 499 pacientes consecutivos elegibles hospitalizados con COVID-19 en estado grave o crítico del 14 de febrero al 24 de marzo de 2020 en el Hospital Leishenshan (Wuhan, China). Se recogieron las características clínicas y los datos de laboratorio y se compararon entre los pacientes que murieron y los que sobrevivieron. Se analizaron las curvas de características operativas del receptor de mioglobina y troponina. A continuación, se dividió a los pacientes en grupo myo+, grupo myo−, grupo tro+ y grupo tro−, y se analizaron las curvas de supervivencia. Los valores pronósticos de la mioglobina y la troponina se analizaron además mediante un análisis multifactorial de Cox. RESULTADOS: La mioglobina y la troponina estaban significativamente elevadas en el grupo de muerte (134,4; rango intercuartílico [RIQ: 24,80; 605] vs. 38,02; [RIQ: 3,87; 11,73] ng/ml; p < 0,001), y la troponina también estaba significativamente elevada en el grupo de muerte (0,01 [RIQ: 0,01; 0,01] vs. 0,04 [RIQ: 0,02; 0,15] ng/ml; p < 0,001). Las curvas ROC demostraron que el área bajo la curva al utilizar la mioglobina para predecir la muerte de los pacientes era de 0,911, con un umbral de 1,17, equivalente al de la troponina. El análisis de supervivencia de Kaplan-Meier reveló una curva de supervivencia significativamente menor en el grupo myo+ que en el grupo myo−. El análisis de supervivencia multifactorial de Cox mostró que la troponina ya no era significativa (HR = 0,98; IC 95%: 0,92-1,03; p = 0,507), pero la mioglobina elevada era un predictor independiente de muerte en los pacientes COVID-19 (HR = 1,001; IC 95%: 1,001-1,002; p < 0,001). El análisis del modelo de Cox para predecir la muerte de los pacientes y el trazado de las curvas de decisión indicaron que el modelo de mioglobina de un solo factor era superior al de la troponina y que el valor predictivo del modelo multifactorial era superior a los análisis de un solo factor. CONCLUSIONES: En los pacientes graves o críticos de COVID-19, la mioglobina y la troponina fueron predictores de la mortalidad y de la probabilidad de conversión a enfermedad crítica, y la mioglobina puede ser superior a la troponina en cuanto al valor predictivo.

Acute kidney injury due to myoglobin cast nephropathy in the setting of coronavirus disease 2019-mediated rhabdomyolysis: a case report.

BACKGROUND: We present this case of coronavirus disease 2019-associated acute kidney injury with rhabdomyolysis-with noteworthy renal biopsy findings demonstrating myoglobin cast nephropathy-to add to the limited literature on coronavirus disease 2019-related acute kidney injury and rhabdomyolysis. CASE PRESENTATION: A 67-year-old Caucasian man presented to our hospital with 3 weeks of malaise and decreased oral intake and several days of abnormal taste, poor appetite, decrease urine output, gastrointestinal symptoms, and myalgias, and was ultimately diagnosed with coronavirus disease 2019. His hospital course was complicated by acute kidney injury and, upon workup of his renal failure, was diagnosed with myoglobin cast nephropathy due to coronavirus disease 2019-mediated rhabdomyolysis. Ultimately, his renal function improved following hydration back to his baseline 6 weeks after his initial diagnosis of coronavirus disease 2019. CONCLUSIONS: Given our limited knowledge of manifestations of coronavirus disease 2019, it is important to have a more in-depth understanding of the spectrum of disease of coronavirus disease 2019, which can affect various organ systems, including the kidney, and the manifestations of end-organ damage associated with it. We present this case to highlight a rarely reported finding of myoglobin cast nephropathy due to coronavirus disease 2019-mediated rhabdomyolysis.

A Highly Sensitive Graphene-based Field Effect Transistor for the Detection of Myoglobin

Biomedical applications adapt Nano technology-based transistors as a key component in the biosensors for diagnosing life threatening diseases like Covid-19, Acute myocardial infarction (AMI), etc. The proposed work introduces a new biosensor, based on Graphene Field Effect Transistor (GFET), which is used in the diagnosis of Myoglobin (Mb) in human blood. Graphene-based biosensors are faster, more precise, stronger, and more trustworthy. A GFET is created in this study for the detection of myoglobin biomarker at various low concentrations. Because graphene is sensitive to a variety of biomarker materials, it can be employed as a gate material. When constructed Graphene FET is applied to myoglobin antigens, it has a significant response. The detection level for myoglobin is roughly 30 fg/ml, which is quite high. The electrical behavior of the GFET-based biosensor in detecting myoglobin marker is ideal for Lab-on-Chip platforms and Cardiac Point-of-Care Diagnosis.

Cardiac Biomarkers of High Risk of Complications and Death in Patients with SARS-COV-2 and CHF

The review is devoted to investigate cardiovascular biomarkers in patients with SARS-CoV-2 associated with a high risk of complications and death. The article provides information on the main cardiovascular biomarkers and pro-inflammatory cytokines in relations to the processes of decompensation in patients with chronic heart failure complicated by ARVI, including the SARS-CoV-2.

'rEACTIVE' MYOSITIS FOLLOWING ANTI-SARS-2 VACCINATION in TWO PATIENTS CARRYING HLA-B∗35 HAPLOTYPE

Background: The anti-SARS2 vaccination is considered the best way to reduce the frequency and the subsequent effects of COVID19 pandemic. To this aim, the most used in western countries are mRNA vaccines BNT16162b2 (Pfzer-Bi-oNT) and mRNA-1273 (Moderna). With both these vaccines the risk/benefts balance is largely favorable and severe adverse effects are almost rare. In keeping, although transient myalgia and arthralgia are frequently seen, myositis have been until now rarely reported. Objectives: To report two cases of myositis occurring in two patients after BNT16162b2 vaccine administration evaluated at the Center for Rheumatic Diseases in Venice, Italy. Methods: In these patients clinical examination, blood and instrumental investigations for myositis and, in addition HLA typing, were performed. Patients were followed for at least six months after the onset of symptoms. Results: The frst patient, a 54-year-old male, complained of high-grade fever 4 days after the I dose of BNT16162b2 (Pfzer-BioNT) followed, by mild fatigue, muscle soreness and increasing weakness. He was sent to the emergency department of the local Hospital. The physical examination confrmed the muscle weakness. Blood investigation revealed an increase of AST: 509 U/L (NV< 37), ALT:189 U/L (NV <78), LDH 609, CPK 11394 U/L (NV<, 309), Myoglobin 3571 ng/ml (VN <96), CRP 1. 6 mg/dl. Prednisone (PN) was started (50 mg orally day) and tapered to 5 mg in two weeks. At high doses, the symptoms slightly improved, but when < 10 mg, all the symptoms reappeared. Thus, he was hospitalized again. The new examination confrmed the increase of all indices of myositis;antinuclear antibodies and myositis antibodies were absent and PN was restarted at 10 mg/day without beneft;echo-cardiography and TC scan were negative. He was then sent to our observation. We increased the dose of PN at 1 mg/PN/kg and we required HLA typing. Two weeks later symptoms disappared almost completely and then we tapered PN 5 mg/day weekly. At present the patients is completely well and muscle indices negative since two months. HLA typing revealed the presence of B∗35 and DRB1∗15. The second case was a 29-year-old female presented with a history of complaints appeared two days after the vaccination with BNT16162b2 administration (Pfzer-BioNT) characterized by three days of high-degree fever, followed by sever weakness, especially in the arms. The family doctor decide to hear our advise. At the initial presentation arm strenght was very decrease and the patient was accompanied. We required a serie of investigations which revealed: CPK 8950 U/L (NV 250), CRP 3.5 mg/dl increased;antinuclear and anti-myositis antibodies absent;cardiac (Ultrasound) and thoracic (CT) investigation and electro-myography negative. HLA typing revealed the presence of haplotypes B∗35 and DRB1∗15. PN (50 mg orally day) was started;two weeks later she improved and both muscle indices and CRP negative. Thus, we reduce the dosage at 25 mg/day with tapering 5 mg weekly. She was completely remitted at end of PN cycle. At present, three month later she is well. Conclusion: The rare occurrence of some particular side effects is not predictable. Our cases of severe myositis which in both cases completely remitted in some months are associated with haplotypes HLA-B∗35 and DRB1∗15. These are both binding sites linked to high-affinity interactions to S-protein T-cell epitope which account for high potentials to trigger immunogenic responses to the S protein of SARS-CoV-2 (1). Furthermore classically, HLA-B35 is associated with reactive arthritis and self-limiting, unclassifed rheumatism (2).

SIGNIFICANT CK ELEVATION IN HEAT-EXPOSURE ADULT RHABDOMYOLYSIS WITH CONCURRENT ASYMPTOMATIC SARS-COV2 INFECTION

CASE: A 59 years old male with past medical history of type 2 diabetes presented in August of 2020 after 2 weeks of leg cramps, nausea, and dark urine that followed several weeks of poor fluid intake during his job as a construction worker. Patient reported that he had a similar episode in 2011, and was diagnosed with rhabdomyolysis with a CK value of 3442. Physical examination revealed a blood pressure of 138/79 mmHg, a pulse of 99 beats/min, respiratory rate of 16 breaths/min, temperature of 36.9 °C, and oxygen saturation of 96% on room air. He was alert and oriented, able to ambulate with pain, and no other significant cardiovascular, pulmonary, neurologic, and gastrointestinal findings. Notable elevation of plasma creatinine of 10.23 mg/dL, BUN of 90mg/dL, sodium of 123 mmol/L, potassium of 5.4 mmol/L, bicarbonate of 15 mmol/L, CRP of 115.4, D-dimer of 4305, Ferritin of 7927, Serum myoglobin of 5320 mcg/L, and total CK of 365148 U/L were noted. Nasopharyngeal swab at presentation was positive for Sars-CoV-2. Patient's urine drug/toxicology screen were negative. The patient was placed on intermittent hemodialysis, and IV fluids were administered. Given his unusually high CK level and COVID-19 positive status, viral myositis associated with COVID-19 was initially suspected. Muscle biopsy showed necrotizing myositis, and ANA titer and myositis specific antibodies were negative. Patient's sole complaint continued to be bilateral lower extremity spasm that gradually improved. The patient was discharged 13 days later with improving kidney functions and total CK of 1683. Patient did not follow up until January of 2021 when he presented to our emergency department for a gunshot wound. His kidney function was back to his baseline at the time. IMPACT/DISCUSSION: Multiple reports in the past 2 years have noted some relationship between rhabdomyolysis and SARS-CoV2 infection, including cases of rhabdomyolysis as a presenting and late complication of severe and mild COVID-19 pneumonia (Valente-Acosta et al, Min et al, and Suwanwongse et a). This case shows both an non- respiratory COVID-19 patient presenting with rhabdomyolysis as well as extremely high presenting CK of 365148 in a non-exercise associated adult rhabdomyolysis. While there are studies that suggests SARS-CoV2 can cause a direct viral injury on muscles, patient's muscle biopsy showing necrotizing myositis rather than direct viral injury suggests that this is not the likely mechanism that aggravated the disease. Rather, given that patient had significantly elevated d-dimer, ferritin, and CRP at presentation, the mechanism may be due to the significant inflammatory responses seen in COVID-19 patients. CONCLUSION: COVID-19 infection, regardless of severity, can significantly exacerbate rhabdomyolysis. Proper inpatient management in such cases can lead to no lasting musculoskeletal or renal complications despite severity. The relationship between COVID-19 infection and severe rhabdomyolysis may be based on the inflammatory responses.

Comparison of the clinical characteristics between 37 adults and 10 children with COVID-19. (Special Issue: Spatio-temporal dynamics analysis, risk assessment and emergency management for COVID-19 epidemic.) [Chinese]

Objective: To explore the differences in clinical characteristics between children and adults with COVID-19. Methods The epidemiological characteristics, clinical symptoms, laboratory results, imaging results and treatment regimens of 37 adult and 10 children cases of COVID-19 were analyzed. Results Family clusters were more common in the adult group, while all children cases were caused by intra-family transmission. The adult group had a significantly higher incidence of symptoms such as fever, cough, pharyngeal pain(pharyngeal itch)and fatigue(muscle soreness)than the children group(P < 0.05), while there is no difference in symptoms like chest tightness and chest pain. The children group had a higher rate of non-changing pulmonary imaging than the adult group(P < 0.05). The children group had higher increase of myocardial enzyme than the adult group(P < 0.05), while there were no differences in the increases of liver enzyme, myoglobin and troponin. The children group had lower increase of CRP, IL-6 and SAA than the adult group(P < 0.05), while there were no significant differences in the increase of PCT and decreases of leukocyte and lymphocyte counts. The treatment regimen for the children group was simpler than that for the adults. Conclusion Intra-family transmission is the main way for children to catch COVID-19. Compared with adults, children have milder clinical symptoms, milder CT lesions, no obvious liver and myocardial damage, and no significant changes in inflammatory indicators.

COVID-19 reinfection: a case report

Protective, sustainable and long-lasting immunity following COVID-19 infection is uncertain, and the potential mechanisms that mediate it are not yet fully understood. We reported a case of a COVID-19 positive 53-year-old female with a medical history of hypertension, vaccination for COVID-19 in July 2021 and paucisymptomatic COVID-19 infection two months later, presented to the ED for an acute uneasy sensation over the posterior left side of the chest with radiation to left arm and shoulder of short duration and a nonproductive worsening cough in the last days. The patient's vital signs were notable for an oxygen saturation of 94% in RT and oxygen therapy was started. An ECG demonstrated sinus tachycardia with diffuse ST elevations. TC pulmonary scan showed a normal parenchimal density and a pericardial effusion. A TTE confermed small pericardial effusion and normal systolic function. CRP, myoglobin, CK-MB and troponin were within the normal values. The anti-spike antibodies were positive and no monoclonal antibody therapy could be performed. She also developed a diarrhea with negative coprocolture and parasitological stool exam. For pericarditis management, high dose steroidal drugs were started. Her symptoms improved rapidily. She was discharged 7 days after the admission. Unfortunately genomic analysis was not available in both episodes and it remains unclear whether they were caused by different strains. Given increased symptom severity during reinfection, our case highlights the need to monitor these patients more closely on a short-term and long-term basis.

Pediatric case of COVID-19 associated rhabdomyolysis

Case Report According to the Center for Disease Control, Severe Acute Respiratory Syndrome Coronavirus 2 (COVID- 19) may present with a wide range of symptoms. Among those, fever, cough, and shortness of breath are commonly present. While COVID-19 associated myalgias is reported as a symptom, we present a case of COVID-19 related rhabdomyolysis. This is a previously healthy 13-year-old obese male who arrived to an outside hospital in respiratory distress after a 1- week history of nasal congestion, productive cough, shortness of breath, emesis and diarrhea associated with malaise and muscle weakness sensation. On presentation he was hypoxic (O2 sat 87%), tachypneic and had increased work of breathing for which was initially treated with 2 liters per minute of oxygen by nasal cannula and fluid resuscitation. The patient had a rapid COVID antigen test that was negative, a chest xray that showed bilateral infiltrates (worse on the right), normal complete blood count and normal electrolytes. However, he was found to have an elevated serum creatinine (1.2), an elevated creatinine kinase level (1264 U/L) and serum myoglobin (97.2 ng/ml) leading to him being diagnosed with acute kidney injury secondary to viral induced rhabdomyolysis and pneumonia. He was treated with antibiotics (Azithromycin and Ceftriaxone) and aggressive fluid resuscitation and transferred to our hospital for further care. At our facility, antibiotics were discontinued after a COVID-19 PCR testing resulted positive. Aggressive fluid resuscitation was continued to treat rhabdomyolysis and he received a course of Remdesivir and Decadron to treat COVID-19 infection. The patient then recovered and was discharged home on the 5th day. Rhabdomyolysis is a life-threatening condition that occurs when muscle necrosis results in the release of its intracellular contents into circulation. In the pediatric population, viral myositis has been reported as a leading cause. It is commonly diagnosed by elevation of serum creatine kinase (CK) and presence of myoglobinuria. Clinically, patients with rhabdomyolysis may be asymptomatic or present with severe disease characterized by myalgias, massive CK enzyme elevations, severe electrolyte imbalances and acute kidney injury. While rhabdomyolysis has previously been reported as a rare complication of COVID-19 infection, there are fewer reports of rhabdomyolysis secondary to COVID-19 in the pediatric population. This case illustrates the importance of suspecting this life threating condition in patients with COVID-19 infection complaining of myalgia or muscle weakness to avoid the severe complications. Of note, while we did not test specifically for the Delta variant, given the time frame of the patient's presentation, we may consider the possibility of COVID-19 Delta variant related rhabdomyolysis.

Compartment syndrome: An unsuspected consequence of hypercoagulable state in a patient with severe covid-19 illness

Introduction Coronavirus 19 (COVID-19) is a viral illness that is caused by SARS-CoV-2. It has a surface spike protein that binds to human angiotensin-converting enzyme 2 receptors expressed in the kidneys, lung, and vascular endothelium. Here we present a case of a 73-year-old critically ill male with COVID pneumonia and acute respiratory distress syndrome (ARDS), who developed compartment syndrome and rhabdomyolysis as a consequence of extensive right lower extremity arterial thrombosis related to a COVID induced hypercoagulable state. Case A 73-year-old COVID positive male with past medical history of coronary artery disease status-post triple coronary artery bypass 10 years ago and type 2 diabetes mellitus presented to the emergency department with progressively worsening dyspnea for one week. His initial oxygen saturation on room air measured 85%, so he was placed on 3 liters per minute supplementation via nasal cannula. CXR showed bilateral diffuse alveolar infiltrates and he was admitted for observation. He developed worsening respiratory failure five days into hospitalization, placed on maximum supplementation via high flow nasal cannula (HFNC), and transferred to the medical ICU. Ultimately, he was intubated and mechanically ventilated for the remainder of his hospitalization due to severe ARDS. After three days in the ICU, his right lower extremity was cold, without palpable nor detectable pulses via bedside Doppler from the femoral to pedal landmarks. Formal ultrasound Doppler that morning confirmed arterial clot extending from the right external iliac to posterior tibial arteries. The patient received embolectomy, stenting, and therapeutic heparin. Within 24 hours, though his creatinine kinase was normal, he developed significantly elevated myoglobin, lactate and worsening acidosis. The patient had a fasciotomy to the right lower extremity at bedside. The next day, he was anuric, with severe acidosis, hyperkalemia, and hypotension, requiring continuous renal replacement therapy (CRRT) and vasopressor support. Discussion Compartment syndrome is characterized by increased pressure within fascial compartments, leading to circulatory compromise, cellular necrosis, and rhabdomyolysis. In this case, the COVID-19 viral effect on coagulation led to extensive arterial thrombosis, complicated by compartment syndrome and renal failure necessitating CRRT. While the exact pathophysiology of the hypercoagulable state in COVID-19 illness is debated, we have observed its manifestations ranging from deep venous thrombosis (DVT), pulmonary embolism (PE), to stroke. Conclusion COVID-19 is known to be a virulent, multifactorial, intelligent virus with myriad end-organ and vascular consequences. When attending to the most critically ill patients with COVID-19, it is wise to consider all forms of vascular thromboembolism.

A case of severe rhabdomyolysis and acute myocarditis in an adolescent female

INTRODUCTION: Rhabdomyolysis describes a condition where muscle tissue destruction occurs. Mortality and morbidity can be significant especially when multi-organ injury ensues. In very few instances, myocarditis has been described in association with this condition. DESCRIPTION: An 11-year-old previously healthy female presents with vomiting, diarrhea, tactile fever, worsening severe bilateral leg pain and gross hematuria for four days. At the Emergency Department, her ECG showed ST depression in lateral leads and abnormal Q waves. Laboratory studies were notable for significantly elevated CK >330,000 U/L. Elevated Troponin T and Troponin I at 3.60 ng/ml and 0.54 ng/mL, respectively. Elevation of CRP 23.5 mg/dl, ALT 1,966 U/L, AST 5,956 U/L, and Ferritin 712.1 ng/ml. Patient had dark brown urine, which was positive for blood, and urine myoglobin peaked at 2690 ng/mL. Her renal function was normal with blood urea nitrogen 8 mg/dl and creatinine 0.4 mg/dl. C3 and C4 levels were decreased, 45 mg/dl and 5 mg/dl, respectively. Anti-dsDNA negative, ANCA negative, and ANA negative. Nasopharyngeal PCR was negative for Mycoplasma pneumoniae, influenza A and B. Blood enterovirus PCR negative. COVID PCR and antibodies negative. Neuromuscular genetic testing was non-diagnostic. Her echocardiography showed thin rim of pericardial effusion and normal ejection fraction. Cardiac MRI demonstrated myocardial edema and regional sub-epicardial delayed enhancement consistent with acute myocarditis. Patient was started on hyperhydration therapy, Solumedrol and intravenous immunoglobulin. The rhabdomyolysis resulted in severe extremity weakness requiring prolonged rehabilitation. Her condition and biomarkers normalized and was subsequently discharged home. Follow up cardiac MRI 6 months later showed increased extracellular volume (ECV) of 38% suggestive of focal and diffuse areas of fibrosis. Patient remains under physical activity restrictions and is being followed by cardiology service. DISCUSSION: Our case highlights severe rhabdomyolysis in association with acute myocarditis and subsequent cardiac structural abnormalities. Although it remains unclear whether myocarditis evolved as a complication of rhabdomyolysis or was triggered by same inciting agent, an infectious etiology overall remains the most likely culprit.

Patients Prognostic value of Troponin-I (Tn-I)

Aim of the study: Aim of the study was to identify an early predictor of poor outcomes in CoViD-19 pneumonia and, in particular, the role of Tn-I. Materials and Methods: An observational retrospective study was performed by analyzing clinical, laboratory and instrumental features from 155 hospitalized patients for CoViD-19 pneumonia in our General Medicine and Semi-intensive Care Units. Results: At the time of hospital admission, 20.3% had an abnormal Tn-I value (cut-off 17.5 ng/l) excluding patients affected by ischemic myocardial injury;10.3% had an abnormal Tn-I excluding also the ones with renal failure (creatinine>1,2 mg/dl). Tn-I was significantly higher in patients transferred to ICU or died (p<0.001), in patients treated by non-invasive ventilation (p=0.007). Tn-I had a positive correlation with NT-proBNP (p<0.001, r=0.353);myoglobin (p=0.020, r=0.232);QTc interval (p<0.001, r=0.301);creatinine (p<0.001, r=0.358);serum proteins in alpha-1 electrophoretic band (p=0.008, r=0.260);FiO2 (p=0.019, r=0.211) and lactate (p=0.11, r=0.229). Tn-I had a negative correlation with pO2 (p=0.029, r=-0.197) and P/F ratio (p=0.033, r=-0.192) on arterial blood gas analysis. In patients with higher Tn-I values, patients were older (p<0,001), had higher creatinine (p<0.001);CPK (p=0.001);inflammation biomarkers were worst (LDH, p=0.002;ESR, p=0.037;CRP, p=0.004;arterial blood gas analysis was worst (lower pO2, p=0.034;lower sO2, p<0.001;higher lactate, p=0.002). Conclusions: Therefore, elevated Tn-I level at admission is a risk factor for the severity and mortality of CoViD-19.

The Predictive Value of Myoglobin for COVID-19-Related Adverse Outcomes: A Systematic Review and Meta-Analysis.

Objective: Cardiac injury is detected in numerous patients with coronavirus disease 2019 (COVID-19) and has been demonstrated to be closely related to poor outcomes. However, an optimal cardiac biomarker for predicting COVID-19 prognosis has not been identified. Methods: The PubMed, Web of Science, and Embase databases were searched for published articles between December 1, 2019 and September 8, 2021. Eligible studies that examined the anomalies of different cardiac biomarkers in patients with COVID-19 were included. The prevalence and odds ratios (ORs) were extracted. Summary estimates and the corresponding 95% confidence intervals (95% CIs) were obtained through meta-analyses. Results: A total of 63 studies, with 64,319 patients with COVID-19, were enrolled in this meta-analysis. The prevalence of elevated cardiac troponin I (cTnI) and myoglobin (Mb) in the general population with COVID-19 was 22.9 (19-27%) and 13.5% (10.6-16.4%), respectively. However, the presence of elevated Mb was more common than elevated cTnI in patients with severe COVID-19 [37.7 (23.3-52.1%) vs.30.7% (24.7-37.1%)]. Moreover, compared with cTnI, the elevation of Mb also demonstrated tendency of higher correlation with case-severity rate (Mb, r = 13.9 vs. cTnI, r = 3.93) and case-fatality rate (Mb, r = 15.42 vs. cTnI, r = 3.04). Notably, elevated Mb level was also associated with higher odds of severe illness [Mb, OR = 13.75 (10.2-18.54) vs. cTnI, OR = 7.06 (3.94-12.65)] and mortality [Mb, OR = 13.49 (9.3-19.58) vs. cTnI, OR = 7.75 (4.4-13.66)] than cTnI. Conclusions: Patients with COVID-19 and elevated Mb levels are at significantly higher risk of severe disease and mortality. Elevation of Mb may serve as a marker for predicting COVID-19-related adverse outcomes. Prospero Registration Number: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42020175133, CRD42020175133.

Myoglobin Offers Higher Accuracy Than Other Cardiac-Specific Biomarkers for the Prognosis of COVID-19.

Although sporadic studies have shown that myoglobin may have better prognostic performance than other cardiac markers in COVID-19, a comprehensive comparative study is lacking. Herein, we retrospectively analyzed the clinical and laboratory data of COVID-19 patients admitted to the Guanggu Campus of Wuhan Tongji Hospital from February 9, 2020 to March 30, 2020, intending to compare the prognostic accuracy of three commonly used cardiac markers on COVID-19 mortality. Our results revealed that abnormal increases in myocardial biomarkers were associated with a significantly increased risk of in-hospital mortality with COVID-19. Interestingly, myoglobin, a non-cardiac-specific biomarker, also expressed in skeletal myocytes, had even higher prognostic accuracy than cardiac-specific biomarkers such as high-sensitivity troponin I (hs-TnI) and creatine kinase-MB (CK-MB). More importantly, multivariate Cox analysis showed that myoglobin, rather than hs-TnI or CK-MB, was independently prognostic for in-hospital mortality in COVID-19. These results were further confirmed by subgroup analyses of patients with severe and critical illnesses and those without a history of cardiovascular disease. Our findings suggest that myoglobin may be a reliable marker of illness reflecting general physiological disturbance and help to assess prognosis and treatment response in patients with COVID-19.